Using somatic cell hybrids between mouse and human cells we have assigned the gene for hexosaminidase B (hex B) to human chromosome 5. Preliminary data from this laboratory strongly suggest that the expression of human hexosaminidase A (hex A) depends on the presense of two asyntenic genes, one on chromosome 5 and the other chromosome 15. Deficiency in hex A activity is associated with Tay-Sachs disease. Deficiency in both hex A and hex B activity is responsible for Sandhoff disease. Using human fibroblasts carrying translocations of autosomes to chromosome 17 we have also assigned the gene for cytoplasmic glutamic oxaloacetic transaminase to the region q24-q ter of human chromosome 10 and we are in the process of determining the order of the genes for mannose phosphate isomerase (MPI), phosphoglucokinase 3 (PGK 3), B macroglobulin and a drain of hex A on chromosome 15.